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METHODS: Fasting serum levels of IL6, IL8, TNFα were measured in 30 cases of T2DM with insulin resistance and 30 cases of T2DM without insulin resistance and 26 normal control subjects by enzymelinked immunosorbent assay.

采用酶联免疫吸附法测定T2DM伴有IR患者30例和不伴有IR患者30例及正常对照26例的空腹血清白细胞介素6(IL6),白细胞介素8(IL8)及肿瘤坏死因子的浓度,并同时测定空腹血糖、糖化血红蛋白(GHbA1c)及空腹胰岛素水平,分析其与IL6,IL8,TNFα的相关性。

Study on the can of making fermented sweet corn in fresh sweet corn;2. The fermentable technique of can of making fermented sweet corn in color sweet glutinous corn and the percentage of can composition were experimented.

以糯米经甜酒曲糖化发酵后的醪液为初始培养基,通过在其中添加各种促生长因子,对益生菌嗜酸乳杆菌的最适生长培养基及培养条件进行了研究。

Our results suggest that the mechanism leading to increased expression of 1-acid glycoprotein and consecutive increased protein binding of atracurium is not mediated by inducible nitric oxide synthase induction and nitric oxide expression.

我们的结论是1-酸糖化蛋白的表达和阿曲库铵与其结合的持续增加不是由诱导性氧化亚氮合酶和氧化亚氮所介导

Plasma concentrations of nitric oxide, atracurium, and 1-acid glycoprotein were measured and acetylcholine receptor numbers were quantified.

氧化亚氮,阿曲库铵,1-酸糖化蛋白和乙酰胆碱受体的数量是确定的。

Resistance to atracurium persisted. 1-acid glycoprotein serum levels remained increased in all CP groups with no differences in acetylcholine receptor expression.

对於阿曲库铵的阻滞是持续的。1-酸糖化蛋白的血浆水平在所有的 CP 组都保持增长并且与乙酰胆碱受体的表达数量无关。

Resistance to atracurium as a result of increased drug binding to 1-acid glycoprotein is associated with increased inducible nitric oxide synthase activity and increased nitric oxide levels in plasma.

对于阿曲库铵的阻滞是由于增加了诱导性氧化亚氮合酶活性和氧化亚氮在血浆中的水平从而使阿曲库铵与1-酸糖化蛋白的结合增加的结果。

Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and Ualbumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

Methods A total of 34 diabetes patients with hypertension were studied. A dose of 5 mg imidapril was given daily in treatment group except oral medicine for decreasing glucose level. Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and Ualbumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

A dose of 5 mg imidapril was given daily in treatment group except oral medicine for decreasing glucose level. Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and Ualbumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

A dose of 5 mg imidapril was given daily in treatment group except oral medicine for decreasing glucose level. Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and U??albumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

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